Retinal Blood Vessel Anomalies Flashcards
1
Q
Minimal systemic workup
A
- Blood pressure, respirations, and pulse (vitals)
- CBC with diff
- Ausculation of carotid arteries. Listening.
2
Q
Low RBC count could indicate
A
Anemia BM failure Kidney disease hemolysis Bleeding Leukemia Malnutrition Vitamin Def Pregnancy Medication
3
Q
High RBC count could indicate
A
Congenital heart disease
Dehydration
Renal cell carcinoma
Polycythemia vera- slow growing blood cancer. BM makes too many–> thickens blood –> Clots –> MI
4
Q
Low WBC count could indicate
A
Severe infections
Meds that destroy WBC
Autoimmune disorders that distort WBC- lupus, RA
Viral infections
Congenial disorders that involve diminished BM function
Reaction to meds
5
Q
High WBC count could indicate
A
An increased production of WBC to fight an infection (bacterial or viral)
Disease of BM causing high production of WBC (leukemia)
Reaction to drug
Autoimmune disease that increases WBC production (RA)
Severe allergic reaction
6
Q
Micro-aneurysms
- How big?
- What is it?
A
50-100 microns in size
Microscopic ballooning of the capillary vasculature. Occurs in a reqs of hypoxia secondary to capillary destruction.
7
Q
Micro-aneurysms are easily observable with ___
A
IVFA
8
Q
Micro-aneurysms result from
A
Acute hypoxia of the deep capillary network.
Layer involved- INL.
9
Q
Patters of Micro-aneurysms
A
focal, local (1), or clustered like grapes on a vine.
10
Q
Can micro aneurysms spontaneously resolve?
A
Yes, may leak at first but later may spontaneously seal secondary to hyalinization.
11
Q
What 3 things are signs of active micro aneurysms leakage?
A
Dot blot hemorrhages, exudate, and edema.
See this? Micro aneurysm have been there a while
12
Q
Expected visual outcomes of Micro-aneurysms
A
Good unless near FAZ
13
Q
Micro-aneurysms treatment options
A
Laser photocoagulation
14
Q
What do Micro-aneurysms look like using IVFA
A
Starry night.
Hyper fluorescing.
15
Q
Macro-aneurysm
-What is it and what area of the retina is it associated with?
A
Isolated ballooning of a larger or major retinal blood vessel. Usually artery or arteriole.
Focal/local blood vessel damage.
Multiple layers of retina may be involved- multi level hemorrhage.
16
Q
3 outcomes of Macro-aneurysms
A
Chronic leakage
Rupture of aneurysm- acute hemorrhage. Can involve multiple layers of retina and vitreous.
Spontaneous resolution- Similar to microaneurysms. They can seal.
17
Q
Visual outcomes of macro aneurysms
A
Depends on location and amount of edema
18
Q
Treatment options for macro aneurysms
A
Depends on location/if macula is involved.
Ex: If in periphery and no VA changes, monitor every 3 months and refer to PCP
Laser or anti veg F
19
Q
Micro aneurysms usually involve the __ capillary network
Macro usually involve ____
A
Deep
Arteries or arterioles found in the NFL (can dip down a bit)
20
Q
3 groups of Idiopathic Juxtafoveal Telangiectasia
A
- Aneurysmal
- Parafoveal
- Occlusive
21
Q
Idiopathic Juxtafoveal Telangiectasia: Aneurysmal (group 1)
- Demographics
- due to what
- Changes to retina/vision
A
Healthy, young males
Abnormal glucose tolerance
Mild to moderate unilateral VA loss with macular cystic changes
22
Q
Idiopathic Juxtafoveal Telangiectasia: Aneurysmal. (group 1)
Ocular findings?
A
- Unilateral macular edema with cystic changes.
- Temporal fovea is involved.
- Telangiectasia- spider like. Dip down at right angle into deeper retina.
- Micro Aneurysms and venule changes
- Lipid deposition (exudate) with chronic leakage
23
Q
How to treat Idiopathic Juxtafoveal Telangiectasia: Aneurysmal. (group 1)
A
Photocoagulation
Anti VEGF therapy
24
Q
Idiopathic Juxtafoveal Telangiectasia: Parafoveal group 2
Presentation?
- Demographics
- Due to what
- unilateral or bilateral
- Compare to IJT group 1
A
Healthy middle age males and females
Due to abnormal glucose tolerance
Bilateral vision loss with macular atrophy
More common and worse prognosis as compared to IJT-1
25
IJT group 2 Parafoveal Ocular findings
Grayish loss of juxafoveal retinal transparency
Temporal early, but then surrounds entire fovea
Fine crystalline depositions and RPE hyperplasia
Micro- A and neovsac with macular edema.
26
IJT group 2 parafoveal treatment options
Anti VEGF
27
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IJT group 3 occlusive
Presentation
-How common?
-Associated with
-Loss of what vision
-How does it affect the ON?
```
Very rare condition with poor VA outcomes
Associated with systemic disease or neurological disease. (polycythemia vera, multiple myeloma, CLL)
Loss of central vision
Ocular atrophy impacts peripheral vision as well.
28
Difference between IJT group 1 and 2
- Demographics
- unilateral or bilateral?
- Amount of VA loss
- Neovasc present?
- How common?
Similarities
```
Group 1:
Males
Unilateral
Vision loss less severe
No novas
Less common
```
```
Group 2:
Males and females
Bilateral
VA loss more severe
Neovasc prob due to ischemia
More common
```
Similarities:
Edema and exudate
Involve macula
Due to glucose intolerance (G3 is more systemic)
29
Collateral blood vessels - What are they and where do they develop?
Difference between collateral and neovasc?
They develop within the framework of the existing vessel network.
May develop vein to vein, artery to artery, or artery to vein.
They are beneficial, unlike neovasc.
30
Collateral blood vessels location in the retina
Located on or within the superficial retina.
31
Collateral blood vessels represent
Past or present regional vascular compromise.
Could be
artery to artery connection (due to artery damage)
Vein to vein connection (due to vein damage)
Artery to vein connection (due to capillary damage)
32
Optocillary shunt
Collateral blood vessels located on the surface of the ON.
Due to:
1. Could be associated with orbital mass. Do MRI to see if it's due to pressure.
2. Could be due to past or present regional vascular compromise.
33
What is congenital shunt vessels or artery-vein communication?
AV communication without capillary obstruction or compromise is a shunt vessel.
Congenital- has alwaysys been there.
No additional testing.
Prob Dx of exclusion.
34
Should collateral vessels leak?
NO! They should not. They are a closed system.
35
What is highly associated with collateral vessels?
Retinal vein occlusion
| or congenital- AV communication/shunt
36
What does IRMA stand for
Intra retinal vascular abnormalities
37
How is IRMA similar to collateral blood vessels?
No leakage
38
What is IRMA
AV connections that BYPASS capillary networks.
Will see fine, irregular, red BV that run from arterioles to venues. They will run over capillary non perfusion due to drop out.
Tells us that there is been capillary drop out.
39
IRMA location
In areas of non-perfusion in diabetic retinopathy only.
40
IRMA is precursor to
Severe diabetic eye disease.
41
How to differentiate between collateral blood vessels and IRMA?
Think IRMA if pt is diabetic
IRMA is arteriole to venule only
Collateral can be artery-artery, vein-vein, or artery-vein.
42
Neovascularization
New blood vessel growth as a response to hypoxia.
Secondary to capillary non-perfusion.
Vessels are weak, leaky, and associated with fibrosis.
Fibrosis develops due to hypoxia and inflammation. Could cause tractional changes.
43
Neovascularization is associated with
Fibrosis and VEGF.
44
Three types of Neovasc
NVI- Neovasc of the iris. At pupillary frill or angle.
NVD- neovasc of the disk. May lead to vitreous hemorrhage. Faces ischemic area. On nerve or 1DD away.
NVE- Neovasc elsewhere. Between junction of perfused to non perfused tissue. Faces hypoxic retina. Multiple layers involved.
45
Neovasc expected retinal findings.
Retinal edema- may be hard to tell where it starts and ends since many layers may be involved.
Hemorrhage- retinal (due to NVE) or vitreous (due to NVD)
Fibrosis and traction- Fibrosis occurs due to hypoxia, inflammation and GF. Neovasc can grow in and around the scar tissue. Overtime, scar tissue shrinks and can pull on the retina. May cause tractional retinal detachment
46
Ischemia leads to the development of
neovasc
47
Gold standard to look at neovasc
IVFA
48
Neovasc
- Visual outcomes?
- Strong association with
- Tx options
Unsure. Depends on acute vs chronic (fibrosis --> traction)
Strong association with uncontrolled systemic disease such as DM. Could also be due to BRVO, CRVO, or hemi retinal occlusion.
Pan retinal laster photocoagulation (PRP)
anti VEGF therapy
49
Which vessels are more likely to become tortuous?
Veins- loosely attached to the retina.
Arteries are more ridged due to muscle and are tightly attached to the retina. Less likely for these to become tortuous.
50
Technology and imaging for collateral blood vessels
IVFA- identify collateral vessels. Should not leak. Could help identify a BRVO.
OCTA- helps identify neovascularlization
Possible MRI if optocilliary shunt- rule out orbital mass.
51
Expected outcomes and resolution of collateral blood vessels
If blood flow is re-established, collateral vessels will regress.
52
Doing IVFA. How long should it take to see initial filling? what if it takes longer>
15-25 seconds. Should be uniform.
If slow, indicates blockage- carotid blockage or hyperlipidemia.
If one quadrant doesn't fill as fast, could be due to BRVO.
53
Difference & similarity between collateral vessels and IRMA
IRMA is arteriole to venule ONLY and exclusive to diabetic eye disease!
Collateral vessels can be artery-artery, vein-vein, or artery-vein.
*Both have no leakage.
54
Diagnostic testing for IRMA
IVFA to identify leaking. If leaking, no IRMA. Prob neovasc.
OCT to identify structural changes in the retina.
OCTA identifies neovasc, IRMA, or collateral.
55
NVI
- Who is susceptible to develop?
- Location
Pts with branch vein occlusion, or pt with significant diabetic eye disease.
Location- Pupillary frill or in angle.
Will see neo
56
NVD
- Location
- Where it is relative to healthy retinal
- Could lead to _____. Why?
On the disc or within 1DD from the ONH.
Neo develops at the boarder of healthy: hypoxic tissue. Faces hypoxic zone.
Could lead to virtual hemorrhage because the ILM is very thin/non existent at the ON. Neovasc could grow into the vitreous, along with fibrosis and bleed.
57
NVE
- Location
- What layers of retina involved?
Anywhere other than iris or on the ONH/within 1 DD
| Multiple layers of retina involved
58
Fibrosis occurs due to which 3 things
Hypoxia, inflammation, and GF.
59
Retinal hemorrhage is likely to happen with what kind of neo?
NVE
60
Virtual hemorrhage is likely to happen with what kind of neo?
NVD- ILM is thin/absent there. Neo can easily enter the vitreous and bleed.
61
Why does neovascularization occur?
When the balance between angiogenesis inhibitors and stimulators is altered. Usually disrupted due to hypoxia.
Ex: BRVO? Off the chart amount of VEG-F released into the retina.
AKA ischemia leads to development of neovasc. (also prob flame shape hems, and CWS)
Look for neo with IVFA.
62
Acquired vein tortuosity is associated with (3)
1. Venous stasis (back flow of blood)
2. Retinal hypoxia
3. Localized vascular occlusion.
63
Acquired vein tortuosity could be due to
BRVO, CRVO, hemi retinal vein occlusion
| Diabetic retinopathy
64
Most common cause of blood vessel tortuosity
Usually congenital
65
How do you know if blood vessel tortuosity is congenital?
If so, expected visual outcomes and treatment options?
Involves extreme changes in all 4 quadrants OU. Involving both veins and arteries.
Good visual outcomes- no changes.
Monitor.
66
Equation to calculate total cholesterol (TC)
TC= HDL + LDL + VLDL
calculate VLDL by triglyceride level divided by 5
67
```
Magic numbers for
TC (total cholesterol)
LDL
HDL
Triglycerides
```
TC (total cholesterol) = less than 200 (can be higher if pt has high HDL levels)
LDL= Less than 100
HDL= 40-60
Triglycerides = less than 150
68
Lipid profile ratio you need to calculate to get good idea of cholesterol level
TC/HDL
If HDL levels are high (which is good), it can make total cholesterol levels look high.
Do this ratio to make sure levels are normal.
Males should be less than 5
Females less than 4.4
69
Vascular sheathing
Congenital vs acquired
-list locations and which vessels it is associated with
Congenital- Artery and vein sheathing is common. Usually located 2DD of the ON or at ON. arteries AND veins involved.
Acquired vein sheathing- Retinal periphery. Looks like a halo. Associated with periphlebitis. (inflammation of outer coat of a vein)
Acquired artery sheathing- Associated with arteriosclerosis. Silver/copper wire appearance.
70
Congenital vascular sheathing
- What vessels are involved
- Location
Artery and vein sheathing is common. Usually located 2DD of the ON or at ON. arteries AND veins involved.
Check to see if there is any sign of papilledema, papillitis, and papillophlebitis. Will see these signs if acquired, but usually congenital.
71
Acquired vein sheathing
- location
- Looks like what?
- Associated with
Retinal periphery. Looks like a halo. Associated with periphlebitis. (inflammation of outer coat of a vein) `
Periphlebitis due to systemic cause such as: posterior uveitis, MS, lupus, Sarcoidosis, pars planets, toxoplasmosis, RP, RVO.
72
Acquired artery sheathing
- Looks like what?
- Associated with
Associated with arteriosclerosis. Silver/copper wire appearance.
73
Lipemia Retinalis
- Due to what
- Appearance and location
Elevated serum triglyceride levels. Can range from 2500-20,000. (Normal is less than 150) Causes retinal blood vessels to fill with lipids= creamy salmon color.
Begins in the periphery then slowly involves vessels in PP.
74
Visual outcomes of lipemia retinals
Asymptomatic, no VA loss. Prob have systemic disease- could have stroke, MI.
Also want to have family members checked- genetic
75
Persistent hyaloid membrane- Bergmeister's papilla
- What is it?
- Location ?
- Symptoms ?
- Prognosis/management
Incomplete regression of the hyaloid artery and embryonic glial sheath. Congenital.
Usually located at the nasal margin.
Asymptomatic.
Good prognosis, no change in VA. Monitor.
76
See persistent hyaloid membrane. Need to rule out what?
PHPV- persistent hyper plastic primary vitreous
Retinoblastoma
ROP- ask about prematurity
77
Pre-papillary vascular loops. What are they? Symptoms ?
Artery or vein?
Bilateral or unilateral?
Congenital.
retinal blood vessel that projects into the vitreous (1.5mm) from the ON and returns to the ON.
usually arterial and unilateral.
True extension of the central retinal artery- independent of bergmeister papillae, but may have glial tissue wrapped around it.
Asymptomatic.
Have pt change gazes, it will move around in the eye.
78
Pre-papillary vascular loop needs to monitored in case it leads to?
What are other differential diagnosis?
Vitreous hemorrhage or RAO
Acquired loops, tumors, or collateral blood vessels.
79
Congenital macrovessels
- What is it?
- Location
- symptoms
Abnormally large retinal vessel that crosses over the horizontal raphe
Usually a vein or venule
Easily observed!
Asymptomatic
80
Congenital macrovessels. Treatment and prognosis
Look for retinal edema if leakage.
OCTA, OCT, IVFA
No treatment unless there is leakage.
Good prognosis, rule out differentials such as Racemose Angioma.
81
Racemose angioma
- What is it?
- Symptoms
Macro vessel that enters and exists the optic nerve.
AV malformation
Large and tortuous vessel.
Symptoms depend on location or hemorrhage. Usually have VA loss and are aware of CNS disorder. Will likely have systemic signs such as seizures/hemiporesis
82
Treatment and prognosis of racemose angioma
Refer to neuro. They also need MRI.
| Usually have symptoms- VA loss or systemic such as seizures.
83
Cilio retinal vessel
- Congenital?
- How common
- ARtery or vein
Congenital, seen in 25% of patients.
| Artery
84
Cilio retinal vessel is derived from what artery
Short posterior ciliary arteries. Rarely choroidal vasculature. AKA blood not coming from central retinal artery- good if there is CRAO.
85
Cilio retinal vessel appearance and symptoms
Hooks out of rim tissue from temporal edge and moves towards the macula.
Completely asymptomatic
